[GITR/GITRL expression in peripheral blood of rheumatoid arthritis]

Beijing Da Xue Xue Bao Yi Xue Ban. 2007 Apr 18;39(2):163-6.
[Article in Chinese]

Abstract

Objective: To explore the expression of GITR/GITRL in rheumatoid arthritis(RA) and its correlation with clinical features of the disease.

Methods: Fifty three RA patients, 35 osteoarthritis (OA) patients and 35 healthy volunteers were included in the study. The real-time-fluorescence quantitative PCR method was used to analyze the expression level of GITR/GITRL mRNA. Using fluorescence-activated cell sorting(FACS), the expression of GITR on CD4+CD25+ T cells in peripheral blood monouuclear cells (PBMC) was detected. The levels of Anti-CCP antibody, C-reactive protein(CRP), erythrocyte sedimentation rate(ESR) and rheumatoid factor (RF) of the RA patients were measured at the same time.

Results: It was shown that the level of GITR/GITRL mRNA and the percentage of GITR+ T cells in the CD4+CD25+ T cell subpopulation[12.38+/-5.72/16.41+/-10.16,(28.12+/-16.85)%] were significantly higher than those of the OA group [9.59+/-5.87/12.09+/-7.53,(21.01+/-14.42)%,P<0.05] and control group [8.75+/-3.78/11.99+/-8.42,(19.98+/- 9.40)%,P<0.05]. The expression of GITR/GITRL from RA patients was positively associated with the level of DAS28 and ESR (r=0.361,r=0.427,P<0.01).

Conclusion: The GITR/GITRL expression of RA patients was higher than that of other groups which may play an important role in the development of RA.

MeSH terms

  • Adult
  • Aged
  • Aged, 80 and over
  • Arthritis, Rheumatoid / blood*
  • CD4 Antigens / metabolism
  • Female
  • Flow Cytometry
  • Glucocorticoid-Induced TNFR-Related Protein
  • Humans
  • Interleukin-2 Receptor alpha Subunit / metabolism
  • Leukocytes, Mononuclear / metabolism*
  • Male
  • Middle Aged
  • RNA, Messenger / biosynthesis
  • RNA, Messenger / genetics
  • Receptors, Nerve Growth Factor / genetics*
  • Receptors, Tumor Necrosis Factor / genetics*
  • Reverse Transcriptase Polymerase Chain Reaction
  • T-Lymphocytes / metabolism
  • Tumor Necrosis Factors / genetics*

Substances

  • CD4 Antigens
  • Glucocorticoid-Induced TNFR-Related Protein
  • Interleukin-2 Receptor alpha Subunit
  • RNA, Messenger
  • Receptors, Nerve Growth Factor
  • Receptors, Tumor Necrosis Factor
  • TNFRSF18 protein, human
  • TNFSF18 protein, human
  • Tumor Necrosis Factors